Figure 4
The ability of electroacupuncture to inhibit myocardial HMGB1 release after ischemia-reperfusion depends on the vagal nerve, but not the sympathetic nerve.
Mice were subjected to 30 min of ischemia and sacrificed after 0 and 24 h of reperfusion. Prior to ischemia, mice were pretreated as described in Fig. 2, except that groups were subjected to unilateral vagotomy (VG), chemical sympathectomy by injection with guanethidine sulfate (GS) or vagal stimulation by injection with neostigmine (Neo). (A–F) Levels of HMGB1 protein were assessed in left ventricle tissue by Western blot (n = 4). (G) Representative images of tissue after 24 h of reperfusion and immunostaining for HMGB1 are shown (n = 3). Arrows indicate HMGB1-positive cells. Scale bar, 50 μm. Data are mean ± SEM. *p < 0.05 vs. IR; #p < 0.05 vs. PC6+IR; &p < 0.05 vs. VG+PC6+IR; $p < 0.05 vs. GS+PC6+IR (A–F: one-way ANOVA followed by Bonferroni correction).
